It is known that the human immunodeficiency virus (HIV) is the etiological agent responsible for AIDS—acquired immune deficiency syndrome, a fatal disease that is characterized by the destruction of the immune system, disabling the organism to react appropriately to life threatening opportunistic infections.
Highly active anti-retroviral therapy (known as HAART) has been used to suppress HIV replication. It consists of the treatment commonly known as anti-AIDS “cocktail”, with at least three active anti-retroviral compounds, containing reverse transcriptase inhibitors, integrase, protease and entry.
However, in infected patients, the virus from reservoirs of CD4+T lymphocyte cells latently infected (i.e. containing residual latent proviral DNA, integrated into the genome of host cells) quickly resumes the viral replication after cessation of the HAART treatment.
Thus, HIV remains a chronic viral infection when such persistent latent infection is not fought.
According to the current rationale in the art, the activation of latent viruses contained in such reservoirs, in the presence of anti-retroviral drugs, intends to make them detectable by the body immune system and accessible to active medication against the virus to cause destruction of cells expressing viral proteins, by reaction of the host immune system and/or such that the cells are brought to apoptosis, inhibiting the replication of viruses that come out from the reservoirs by action of the anti-retroviral drugs, thus exhausting the reservoir of HIV persistent infection and enabling the total eradication of the infection.
In other words, the selective induction of latent infection allows anti-retroviral drugs and the antiviral immune response to access and eradicate residual HIV infection—i.e. not just temporarily stabilizing the immune system without later use of anti-retrovirals, but definitely suppressing the HIV infection in the human body.